Unilateral sensorimotor contusion injury results in contralateral hindlimb paralysis as well as behavioral & cognitive deficits in rats. In response to cortical injury, adult neural stem cells (NSC) in the subventricular zone (SVZ) proliferate, and generate new neurons & glia that migrate towards injured areas. Thus, they may
potentially be harnessed for neural repair. After cortical injury, the number of migratory NSC’s to lesioned sites has been shown to be significantly lower than the overall cell loss in rats.
To address this issue, in-vitro & in-vivo studies have shown that various growth factors (GF) enhance the rate of proliferation, differentiation & migration of NSC’s within the SVZ, as well as the rostral migratory stream (RMS).
The present study is an attempt to accelerate recovery of behavioral & cognitive functions from
cortical TBI via a single injection of matrigel containing GF immediately after somatosensory contusion in adult rats. Each injection (containing 100ng GF/60mcL matrigel) was made such that a continuous stream of gel was formed from the region of the RMS (rostral to genu of the corpus callosum) to the site of injury.
Assessment of behavioral & cognitive tasks began 7 days post surgery. Fourteen days of Morris Water
(i.e., moving hidden platform - 8 trials a day) & 7 days of Rod task (4 trials a day) testing revealed that lesioned animal which received the FGF or EGF treatment performed as well as sham & significantly better than lesioned control groups.
Similarly, animals who received combination of all 3 GFs performed better than lesion control groups on both tasks, however not as well as sham, the FGF or EGF-treated groups. VEGF- treated animal performed similarly to lesion/no treatment animals.
Overall, this study shows that the intracerebral injection of certain neurotrophic factors accelerates the recovery of behavioral & cognitive skills in cortical injured rats.
Potential mechanisms for acceleration of functional recovery could involve their
recruitment & directed migration of NCSs from the RMS to the site of cortical injury and/or local neuroprotective effects of the growth factors.